Clinical and pathological evidence suggests the existence of a diabetic cardiomyopathy. Therefore, an animal model was creatd to study the effect of diabetes on myocardial function. Ten female Wistar rats (D) (weight 194 plus or minus 3 gms, age 9 wks) were made diabetic by i.v. injection of streptozotocin(60 mg/kg); serum glucose 3 wks later was 491 plus or minus 33 mg%. Four weeks after injection 10LV papillary or trabecular muscles were studied isometrically; 10 age-matched controls (C) were also studies. All values given below were obtained at the muscle length where developed tension (DT) was maximal. At study, body weight was lower in D (198 plus or minus 8 (D), 252 plus or minus 5 gms (C)). Heart weights were also lower (.58 plus or minus .03 (D), .70 plus or minus .02 gms (C)); however, heart to body weight ratios were the same. There were no significant differences in resting tension or compliance, DT, or the peak of tension rise (plus T max). The length-dependence (variation as muscle length was changed) and response to increase extracellular (Ca ions) (0.6 ti 2.4 mM/L) of DT was less in D. The peak rate of tension fall (minus T max) was less in D at high (Ca ions) (27.55 plus or minus 3.26 (D), 41.80 plus or minus 5.77 gm/mm2/sec (C)) only. The length dependence and response to increased (Ca ions) of minus T max was less in D. Negative T max, normalized for DT was significantly lower in D at either (CA ions). Time to peak tension was slightly longer in D at either (Ca ions). T 1/2 of relaxation (time to 50% fall of DT) was markedly longer in D at either (Ca ions) (127 plus or minus 7 (D), 88 plus or minus 3 msec (C) at high (Ca ions). Thus, 4 weeks of diabetes resulted in marked prolongation of isometric relaxation. Diabetic muscles also showed differences in the length-dependence and Ca ions responsiveness of contraction and relaxation indexes. These changes may represent early manifestations of a diabetic cardiomyopathy in rats.